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العنوان
Relationship of ghrelin and leptin Hormones with Body Mass Index in obesity
الناشر
Moataz Mohamed Hussein Ahmed
المؤلف
Ahmed,Moataz Mohamed Hussein
هيئة الاعداد
مشرف / Heba Allah Mostafa Kamal
مشرف / Nevin Ezz El Din Al Abd
مشرف / Nadida Abd Al-hamid Gohar
مشرف / Ahmed,Moataz Mohamed Hussein
تاريخ النشر
2012
عدد الصفحات
115
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب (متفرقات)
تاريخ الإجازة
1/1/2012
مكان الإجازة
جامعة القاهرة - كلية الطب - Clinical and Chemical pathology
الفهرس
Only 14 pages are availabe for public view

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Abstract

The increase in childhood obesity, has promoted research into mechanisms of appetite regulation. Complex pathways modulate energy balance, involving appetite centres in the hypothalamus.
Hormonal signals of energy status released by the gut &by the periphery ,better understanding of appetite regulation improve understanding of the aetiology of obesity and hence offer potentially useful treatment of obesity (Archives of disease in childhood, 2006).
Ghrelin is synthesized predominantly by the stomach . It is the endogenous ligand for the growth hormone receptor which is expressed in the brain stem and hypothalamic nuclei . A role of ghrelin in the aetiology of human obesity has been proposed (Kojima et al., 1999).
Ghrelin levels are lower in obese subjects compared to lean, and weight loss result in an increase in ghrelin level, which may contribute to difficulties in maintaining the reduced weight. Food fails to suppress Ghrelin levels in obese humans, which again impair postprandial satiety and contribute to overeating (English et al., 2002).
Leptin is synthesized in white adipose tissue and circulates at concentration proportional to body fat mass. The adipose hormone leptin is the protein product of the obese (ob) gene (Zhang et ai., 1994).
Food restriction lower leptin levels and this is reversed by refeeding .It is thought that the main function of leptin is to signal starvation when levels are low, conversely high levels signal the levels of body fat stores to the CNS in an environment of nutritional plenty (Ahima,et al., 1996).